Heart failure is an important and wisespread health problem. Further, it is generally held that this disease is probably complex in its pathogenesis and involves a variety of malfunctioning cellular systems. It follows then that more complete knowledge of these cellular systems is necessary before a full understanding of heart failure may be gained. To date no in-depth information exists as to the possible role of the Na-K pump in the disease. This work will help to elucidate the role of the sodium-potassium pump in the pathogenesis of heart failure. A possible link between reduced activity of this membrane enzyme and the lowered state of inotropy in heart failure may be established. It is also anticipated that a mechanism for reduced pump function in heart failure could be revealed. Underlying pump malfunction and associated reduced inotropy may be morphological, biochemical, and electrophysiological phenomena. Knowledge of the above mentioned relationship may be instrumental toward revealing means of retardation or reversal of the disease process leading to heart failure. This project offers several novel approaches toward achieving its goals. A unique method for electrophysiological quantiation of Na-K pump activity has been developed. A new approach toward examining cell volume is employed which will allow for simultaneous studies of pump activity, inotropy, and cell volume in functioning, intact papillary muscles. A first attempt will be made to compare directly the properties of the electrophysiological Na-K pump with those of biochemically determined sarcolemmal ATPase. Novel use of osmometric interventions will be used to further elucidate mechanisms in heart failure and possibly suggest means of reversal.